User:Prikale/New sandbox

Article body: Post Traumatic Stress Disorder (PTSD)
"Post-traumatic stress disorder (PTSD) is a stress-related mental health disorder that emerges in response to traumatic or highly stressful experiences. It is believed that PTSD develops as a result of an interaction between these traumatic experiences and genetic factors. Evidence suggests epigenetics is a key element in this. The hypothalamus-pituitary-adrenal (HPA) axis plays a key role in stress response. Based on several findings, the HPA axis appears to be dysregulated in PTSD. A common pathway dysregulated in HPA axis involves a hormone known as glucocorticoid and its receptor, which aid in stress tolerance by downregulating stress response. Dysregulation of glucocorticoid and/or glucocorticoid receptor can disrupt stress tolerance and increase risk of stress-related disorders such as PTSD. Epigenetic modifications play a role in this dysregulation, and these modifications are likely caused by the traumatic/stressful experience that triggered PTSD."

Draft Edit -- "Post-traumatic stress disorder (PTSD) is a stress-related mental health disorder that emerges in response to traumatic or highly stressful experiences. It is believed that PTSD develops as a result of an interaction between the stress associated with these traumatic experiences and genetic factors. Evidence suggests epigenetic factors are also a a key element in this. Specifically, there is evidence suggesting PTSD formation can cause downstream epigenetic pathways resulting in "fear extinction, DNA methylation and acetylation of histone proteins." ...The hypothalamus-pituitary-adrenal (HPA) axis plays a key role in stress response. Based on several findings, the HPA axis appears to be dysregulated in PTSD. A common pathway dysregulated in HPA axis involves a hormone known as glucocorticoid and its receptor, which aid in stress tolerance by downregulating stress response. Dysregulation of glucocorticoid and/or glucocorticoid receptor can disrupt stress tolerance and increase risk of stress-related disorders such as PTSD. ''In the hippocampus of stressed animals, the 3′-UTR, untranslated region of mRNA, of the glucocorticoid receptor was hyper-hydroxymethylated which led to increased transcription and thus, the disruption of stress tolerance and increased risk of disorders such as PTSD. This reaction differs between short-lived exposure to stress and chronic exposure in that the same transcription factor has its promoter inhibited in chronic stress. These distinctions are important in understanding the epigenetic patterns of stress and genetic interactions with PTSD triggers. Epigenetic modifications play a role in this dysregulation, and these modifications are likely caused by the traumatic/stressful experience that triggered PTSD... Treatments for PTSD are targeted around DNA methylation and mitigating the observed increase. Increased methylation due to impaired TET protein regulation leads to fear extinction incapabilities and ultimately unsuccessful exposure therapy for patients. Successful fear extinction is characterized by decreased levels of HDAC activity and DNA methylation both of which are regulated by a working TET1 gene and enzyme. The observation of epigenetic modifications on changes to fear learning is an active area of research as Stress-enhanced fear learning (SEFL) paradigms and are an important tool for forming preclinical models of PTSD ''. ''A specific tool, cited by Blouin, is the single-prolonged stress (SPS) model in which a complex stressor is consistently presented. This is used to explore the complexity of PTSD, particularly its impaired fear extinction."''